Literature DB >> 9731990

Decreased prevalence of Helicobacter pylori infection in gastroesophageal reflux disease.

R V Varanasi1, G T Fantry, K T Wilson.   

Abstract

BACKGROUND: An increased incidence of reflux esophagitis has been reported after eradication of H. pylori in patients with duodenal ulcer. To determine if H. pylori is associated with lower rates of esophagitis, we studied the prevalence of H. pylori infection in patients with and without reflux esophagitis and a subgroup of patients with concomitant peptic ulcer disease.
METHODS: Patients who underwent esophagogastroduodenoscopy and had diagnostic testing for H. pylori over a 30-month period were studied. H. pylori infection was determined by rapid urease testing, gastric histopathology, or serology. Reflux esophagitis was determined by endoscopic and/or histologic criteria.
RESULTS: Of 514 patients, 39.5% had H. pylori infection and 22.2% had reflux esophagitis. The prevalence of H. pylori infection in patients with reflux esophagitis was 30.7%, compared with 42.0% in patients without esophagitis (p = 0.039). The odds ratio for esophagitis risk with H. pylori infection was 0.61 (95% CI, 0.39-0.95). Neither patient age nor gender affected H. pylori prevalence. In patients with duodenal ulcer, H. pylori was present in 36.4% of patients with esophagitis and in 69.2% of patients without esophagitis (p = 0.018). The odds ratio for esophagitis with H. pylori infection in these patients was 0.25 (95% CI, 0.09-0.73).
CONCLUSIONS: Our study demonstrates that H. pylori infection is significantly less prevalent in patients with reflux esophagitis and may protect against its development. In duodenal ulcer patients, this effect was more dramatic. Further study is required to confirm these findings and elucidate mechanisms underlying possible beneficial effects of H. pylori.

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Year:  1998        PMID: 9731990     DOI: 10.1046/j.1523-5378.1998.08001.x

Source DB:  PubMed          Journal:  Helicobacter        ISSN: 1083-4389            Impact factor:   5.753


  19 in total

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9.  Helicobacter pylori induces apoptosis in Barrett's-derived esophageal adenocarcinoma cells.

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10.  L-arginine availability regulates inducible nitric oxide synthase-dependent host defense against Helicobacter pylori.

Authors:  Rupesh Chaturvedi; Mohammad Asim; Nuruddeen D Lewis; Holly M Scott Algood; Timothy L Cover; Preston Y Kim; Keith T Wilson
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